Assistive Devices to Improve Independence

Assistive devices for independence are available to aid in mobility/ambulation (ambulatory aids), activities of daily living (ADLs) and self-care, as well as for voice, hearing, vision, and safety. Ambulatory aids (eg, canes, crutches, walkers) are used to provide an extension of the upper extremities to help transmit body weight and provide support for the patient. The image below provides some examples of ambulatory aids.
1: Adjustable aluminum cane. 2: Unadjustable aluminum cane. 3: T-top cane. 4: Quad cane. 5: Walk cane (hemi-walker). Assistive devices for ADLs, as well as for self-care and leisure activities, range from simple objects for daily use (eg, plate guards, spoons with built-up handles, elastic shoelaces, doorknobs with rubber levers) to complex electronic devices, such as voice-activated environmental control systems.

Category

Assistive devices to improve independence

Device details

Canes

• C cane
• Functional grip cane
• Quad cane (narrow [small] based and wide [large] based)
• Walk cane (hemi-walker)
• Visual impairment cane

Crutches

• Axillary (underarm) crutches
• Nonaxillary (forearm [Lofstrand, Canadian]) crutches
• Crutches with orthoses (wooden forearm orthosis, platform forearm orthosis, triceps weakness orthosis [Warm Springs crutch, Everett crutch])

Crutch gaits

• Four-point, 3-point, and 2-point gaits
• Swing-through gaits
• Swing-to gaits
• Drag-to (tripod) gait

Walkers

• Standard (pickup) walker
• Rolling (4-wheeled) walker (with or without a seat)
• Front-wheeled walker
• Reciprocal walker
• Forearm support walker
• Stair-climbing walker
• Heavy-wheeled walker with foldaway seat and removable back

Brain-computer interface/motor neuroprosthetic devices
Cyberkinetics

• BrainGate
• BrainGate 2

Electrolarynges

• Neck electrolarynx
• Intraoral electrolarynx

Botulinum Toxin in Pain Management

 
Diagnosis and treatment of painful muscle syndromes can be a difficult and frustrating task for any clinician. Typically, the mainstay of therapy for such conditions is therapeutic exercise, analgesics, and a tincture of time. Unfortunately, not all patients respond to this paradigm, and, despite heroic efforts on the part of the treating clinician, some conditions are refractory to this approach.
Reports have described the purported effectiveness of using a biologic neuromuscular blocking agent, botulinum toxin, in the treatment of painful conditions associated with skeletal muscle. While incompletely understood and at times controversial, use of botulinum toxin in the treatment of conditions associated with involuntary muscle contraction, such as focal dystonia and spasticity, is supported by prospective, randomized clinical research; however, while the volume of comparable studies in pain syndromes is growing, the number of clinical randomized trials is limited. Moreover, not all such reports have demonstrated clear efficacy of the use of botulinum toxin under all circumstances. Therefore, in view of our current understanding of the nature of muscle-induced pain and the paucity of prospective research regarding neuromuscular blockade and/or inhibition of nociception in such conditions, critical and careful analysis of the data and opinions presented in this section is appropriate.
This article provides general direction and practical details for the clinician considering botulinum toxin for treatment of pain. Anatomic drawings for injection localization and dosing information are intended only as general guidelines; therapy with botulinum toxin always must be individualized, accounting for the patient's needs and the clinician's expertise. In addition, information presented should be used as a convenient reference source, not as a substitute for clinical training in the use of botulinum toxin.

Epidural Steroid Injections

Epidural steroid injections (ESIs) have been endorsed by the North American Spine Society and the Agency for Healthcare Research and Quality (formerly, the Agency for Health Care Policy and Research) of the Department of Health and Human Services as an integral part of nonsurgical management of radicular pain from lumbar spine disorders.
Radicular pain is frequently described as a sharp, lancinating, radiating pain, often shooting from the low back down into the lower limb(s) in a radicular distribution. Radicular pain is the result of a nerve root lesion and/or inflammation. Clinical manifestations of nerve root inflammation include some or all of the following: radicular pain, dermatomal hypesthesia, weakness of muscle groups innervated by the involved nerve root(s), diminished deep tendon reflexes, and positive straight or reverse leg–raising tests. In contrast to oral steroids, ESIs offer the advantage of a more localized medication delivery to the area of affected nerve roots, thereby decreasing the likelihood of potential systemic side effects. Studies have indicated that ESIs are most effective in the presence of acute nerve root inflammation.
The first documented epidural medication injection, which was performed using the caudal approach (see Approaches for Epidural Injections), was performed in 1901, when cocaine was injected to treat lumbago and sciatica (presumably pain referred from lumbar nerve roots).^[1] According to reports, epidurals from the 1920s-1940s involved using high volumes of normal saline and local anesthetics. Injection of corticosteroids into the epidural space for the management of lumbar radicular pain was first recorded in 1952.
ESIs can provide diagnostic and therapeutic benefits. Diagnostically, ESIs may help to identify the epidural space as the potential pain generator, through pain relief after local anesthetic injection to the site of presumed anatomic pathology. In addition, if the patient receives several weeks or more of pain relief, then it may be reasonable to assume that an element of inflammation was involved in his or her pathophysiology. Since prolonged pain relief is presumed to result from a reduction in an inflammatory process, it is also reasonable to assume that during the period of this analgesia, the afflicted nerve roots were relatively protected from the deleterious effects of inflammation. Chronic inflammation can result in edema, wallerian degeneration, and fibrotic changes to the neural tissues.
In these authors' opinion, ESIs are best performed in combination with a well-designed spinal rehabilitation program. In most cases, epidural injections should be considered as a treatment option after other treatment attempts (eg, physical therapy, including therapeutic exercise, manual therapy, and medications) have failed to improve the patient’s symptoms. However, ESIs may be indicated earlier in the treatment algorithm in some selected patients. Examples might include patients with medical contraindications to certain oral analgesics and patients whose pain severity substantially limits their ability to appropriately engage in therapeutic exercise.
A variety of approaches can be used to inject corticosteroids into the epidural space (see Approaches for Epidural Injections). For purposes of this article, the authors generally refer to all epidural steroid injections as ESIs, only specifying the specific type of approach if needed for a point of distinction or clarification.

Massage, Traction, and Manipulation

Various forms of massage, traction, and manipulation have been used in medicine throughout the world for several thousand years. Each modality represents an approach to treatment of the musculoskeletal and other systems sought by a steadily increasing number of people. While research on each of these modalities continues, a long-standing variable, the concept of touch, unites them all.
In the 1940s, Rene A. Spitz reported on foundling home infants who, otherwise healthy and well taken care of, failed to thrive and often died in the absence of being held or touched. Kunz and Krieger additionally defined and taught the principles behind the related concepts of healing touch and therapeutic touch in the 1970s. While there is no consensus on the complete physiology of massage, traction, or manipulation, it is generally accepted that there is more to these treatment approaches than just the interaction of mechanical forces and human anatomy. There is a long history of touch as a natural, essential component to healing and health maintenance.
Throughout history, massage has been woven into the cultural context of medicine. Massage may be the earliest and most primitive tool to treat pain.^[1] Massage consists of Eastern and Western variants. In the West, the practice and popularity of massage has varied over time. In recent years, a previous decline in popularity of massage, probably related to technological advancements in medicine, has been reversed into a resurgence of interest. In the US, approximately $2-4 billion is spent annually on visits to massage therapists, which accounted for approximately 26% of the $11.7 billion spent on nontraditional healthcare in the 1990s.
The American people are pursuing massage in increasing numbers for various reasons (eg, relief of pain, relaxation, conditioning). While little doubt exists that massage is beneficial for certain conditions, additional research is needed to establish its profile of efficacy.

Definition of basic massage concepts

Massage is a therapeutic manipulation of the soft tissues of the body with the goal of achieving normalization of those tissues. Massage can have mechanical, neurological, psychological, and reflexive effects. Massage can be used to reduce pain or adhesions, promote sedation, mobilize fluids, increase muscular relaxation, and facilitate vasodilation. Massage easily can be a preliminary treatment to manipulation; however, it clearly targets the health of soft tissues, while manipulation largely targets joint segments.
Massage consists primarily of hand movements, some of which may be traction based. Traction is defined as the act of drawing or pulling or as the application of a pulling force. Traction sometimes involves equipment but also can be applied manually. In addition, traction affects changes in the spinal column itself, with soft tissues only secondarily changed. Effects of massage, like those of traction, tend to be fairly nonspecific.

Western massage

Western massage is the chief type of massage practiced in the United States today. Among the most common types of massage therapy are acupressure (Shiatsu), Rolfing, Swedish massage, reflexology, and release.^[1] Western massage organizes variations of soft-tissue manual therapy into several categories. Pare of France introduced the basic terminology for Western massage to the United States. The essence of Western massage is use of the hands to apply mechanical forces to the skeletal muscles and skin, although the intent may be to affect either the more superficial tissues or the deeper ones. Types of basic Western massage are characterized by whether (1) the focus of pressure is moved by the hands gliding over the skin (ie, effleurage), (2) soft tissue is compressed between the hands or fingers and thumb (ie, pétrissage), (3) the skin or muscle is impacted with repetitive, compressive blows (ie, tapotement), or (4) shearing stresses arecreated attissueinterfaces below the skin (ie, deep friction massage). Forms of Western massage include the following:

• Effleurage

  • In this approach, the practitioner's hands glide across the skin overlying the skeletal muscle being treated.
  • Oil or powder is incorporated to reduce friction; hand-to-skin contact is maintained throughout the massage strokes.
  • Effleurage can be superficial or deep.
  • Light strokes energize cutaneous receptors and act by neuroreflexive or vascular reflexive mechanisms, whereas deep stroke techniques mechanically mobilize fluids in the deeper soft-tissue structures.
  • Deep stroking massage is performed in the direction of venous or lymphatic flow, whereas light stroking can be in any direction desired.
  • Effleurage may be used to gain initial relaxation and patient confidence, occasionally to diagnose muscle spasm and tightness, and to provide contact of the practitioner's hands from one area of the body to another.
  • The main mechanical effect of effleurage is to apply sequential pressure over contiguous soft tissues so that fluid is displaced ahead of the hands as tissue compression is accomplished.
• Pétrissage

  • Pétrissage involves compression of underlying skin and muscle between the fingers and thumb of 1 hand or between the 2 hands.
  • Tissue is squeezed gently as the hands move in a circular motion perpendicular to the direction of compression.
  • The main mechanical effects are compression and subsequent release of soft tissues, reactive blood flow, and neuroreflexive response to flow.
  • Lymphatic pump is a type of pétrissage done to the chest and rib cage of persons with respiratory compromise in order to draw lymph into the thoracic duct and venous circulation as a result of an alternating increase and decrease of pressure on the chest cavity.
• Tapotement

  • This percussion-oriented massage involves striking soft tissue with repetitive blows, using both hands in a rhythmic, gentle, and rapid fashion.
  • Numerous variations can be defined by the part of the hands making an impact with the body.
  • The therapeutic effect of tapotement may result from compression of trapped air that occurs on impact.
  • The overall effect of tapotement may be stimulatory; therefore, healthy persons with increased tolerance for this approach are more likely to find this type of massage useful.
• Deep friction

  • Pressure is applied with the ball of the practitioner's thumb or fingers to the patient's skin and muscle.
  • The main effect of deep friction massage is to apply shear forces to underlying tissues, particularly at the interface between 2 tissue types (eg, dermis-fascia, fascia-muscle, muscle-bone).
  • Deep pressure keeps superficial tissues from shearing so that shear and force are directed at the deeper tissue surface interface.
  • Deep friction massage frequently is used to prevent or slow adhesions of scar tissue

Eastern massage

Over the centuries, Eastern massage systems have been an integral part of the cultures where they are practiced. Systems for evaluation, diagnosis, and treatment generally are not grounded in conventional Western neurophysiology. Eastern massage includes, among other approaches, Shiatsu, a Japanese system based on traditional Chinese meridian theory with principles of Western science. The theory of Shiatsu is based upon the system of the 12 traditional Chinese meridians (ie, major channels) of the body in which the energy, life force, or Chi, circulates. Acupressure pressure points, situated along the course of channels, allow access to these channels. Acupressure applies massage forces, largely through digital pressure, to the same points treated with acupuncture needles. Imbalances of energy along the meridians are believed to cause disease and can be rectified by localized finger pressure.

Reflexology and auriculotherapy

• These systems of massage share the meridian concept with Shiatsu.
• In these approaches, the meridians are believed to have whole body representations on the extremities (similar to the homunculus of the brain).
• The feet (in reflexology) and the ear (in auriculotherapy) have been mapped in detail.

Decongestive Lymphatic Therapy

Decongestive lymphatic therapy is the complex massage approach that includes manual lymphatic drainage (MLD) in addition to compressive bandages, exercises, and skin care. Manual lymphatic drainage consists of gentle massage in the treatment of lymphedema. Proximal areas are treated first to prevent a damming effect; the treatment is thought to stretch the lymphatic collectors and to stimulate the drainage system. The massage is followed by the application of compressive bandages and is incorporated into a complete self-care program.

Massage technique

The practitioner controls several variables of massage, including milieu. Actual application of treatment includes rhythm, rate, pressure, direction, and duration.
Most massage approaches involve a friction-reducing medium, so that the hands of the practitioner move along the patient's skin with minimal friction. Powders or oils often are used. Massage strokes also should be regular and cyclic. The rate of application for massage varies with the type of technique. In some approaches (eg, tapotement, percussion), the rate is several times per second, while in others it is much slower.
The amount of pressure depends upon technique and desired results. Light pressure may produce relaxation and relative sedation and may decrease spasm; breakdown of adhesions and intervention at a deeper tissue level may require heavier pressure. Treatment of edema and stretching of connective tissue generally requires intermediate amounts of pressure. Direction of massage often is centripetal to provide better mobilization of fluids toward the central circulation. The sequence of tissues treated often is performed in a centripetal fashion.
When muscles are treated, motions generally are kept parallel to muscle fibers. If the treatment goal is to reduce adhesions, shearing forces are circular or at least include cross-fiber components. The area to be treated with massage depends upon the condition being treated and may vary from a well-circumscribed area to treatment of contiguous areas.
Duration of treatment depends upon the area being treated, desired therapeutic goals, and patient tolerance. Wide variation exists regarding treatment duration, which often is guided by changes occurring to tissue during massage application. If massage is performed before other treatments, duration may be determined by the result needed in order to optimize the next treatment step. Duration of a massage therapy program can range from 1 week to months and depends upon verifiable therapeutic goals. Patients must be reexamined from time to time, depending upon diagnosis and therapeutic goals, to insure satisfactory progress.

Nonoperative Treatment of Osteoporotic Compression Fractures Overview of Osteoporotic Compression Fractures

Osteoporosis and osteoporotic vertebral compression fractures are commonly encountered clinical problems. The definition of osteoporosis is diminished bone density measuring 2.5 standard deviations below the average bone density of healthy, 25-year-old, same-sex members of the population. In the United States, approximately 35% of women older than 65 years have osteoporosis.
Vertebral compression fracture (seen in the image below) is the most common complication of osteoporosis. More than 700,000 new vertebral compression fractures occur every year in the United States alone, accounting for more than 100,000 hospital admissions and resulting in close to $1.5 billion in annual costs.
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Anteroposterior and lateral radiographs of an L1 osteoporotic wedge compression fracture. Most of patients experiencing an osteoporotic vertebral compression fracture remain asymptomatic or minimally symptomatic; however, a large number of these patients do experience significant pain, resulting in decreased quality of life and disability. Conventional medical treatment for these patients includes pain medication, activity limitation, physical therapy, and (possibly) bracing.^{[1, 2]}
Patients with osteoporotic vertebral compression fractures are usually treated nonoperatively.

Types of vertebral compression fractures

Vertebral compression fractures characteristically demonstrate a wedge-shaped pattern (seen in the images below) with gross collapse of the anterior portion of the vertebral body and relative preservation of the posterior body height.
Anterior wedge compression fracture with an intact posterior vertebral cortex. Osteoporotic spine. Note the considerable reduction in overall bone density and the lateral wedge fracture of L2. A second common form of fracture is a central crush fracture, which frequently occurs in the lower lumbar spine. Increased interpedicular space, involvement of the posterior cortex, or laminar fracture suggest a burst fracture (seen in the image below), which may be unstable.
A vertebral burst fracture.

Etiology of osteoporotic compression fractures

Cortical and trabecular bone loss, as well as disruption of the microarchitecture of bone, are all typical of osteoporosis. Spinal flexion and axial compression have been shown to place maximal stress on the superior endplate of the vertebral body. The asymmetry of the vertebral body produces maximal stress at the anterior aspect of the cortical shell.
A combination of these factors, that is, decreased, asymmetrical, and irregular bone density, is a hallmark of osteoporotic bone loss. Coupled with even minimal flexion and/or axial loading, these factors predispose the osteoporotic vertebrae to wedge-shaped compression fractures, acquired kyphosis, and general height loss.
Once 1 vertebral compression fracture has occurred, a biomechanical environment is created that favors additional fractures. This occurs as a result of the vertebral compression fracture causing an additional kyphosis, shifting the patient's center of gravity anteriorly and producing a longer moment arm. This longer moment arm increases kyphotic angulation and places additional stress on the vertebrae, particularly the vertebrae adjacent to the primary fracture.
Progressive kyphosis, additional fractures, and neurologic changes are potential complications of osteoporotic compression fractures. These complications can be minimized with appropriate, expeditious care.
All vertebral compression fractures require a systematic examination to rule out an underlying systemic illness, such as malignancy, infection, or renal or liver disease.

Therapeutic Exercise

DeLateur defined therapeutic exercise as bodily movement prescribed to correct an impairment, improve musculoskeletal function, or maintain a state of well-being.^[1] It may vary from highly selected activities restricted to specific muscles or parts of the body, to general and vigorous activities that can return a convalescing patient to the peak of physical condition. Therapeutic exercise seeks to accomplish the following goals:

• Enable ambulation
• Release contracted muscles, tendons, and fascia
• Mobilize joints
• Improve circulation
• Improve respiratory capacity
• Improve coordination
• Reduce rigidity
• Improve balance
• Promote relaxation
• Improve muscle strength and, if possible, achieve and maintain maximal voluntary contractile force (MVC)
• Improve exercise performance and functional capacity (endurance)

The last 2 goals mirror an individual's overall physical fitness, a state characterized by good muscle strength combined with good endurance. No matter which types of exercise may be needed initially and are applied to remedy a patient's specific condition, the final goal of rehabilitation is to achieve, whenever possible, an optimal level of physical fitness by the end of the treatment regimen.

Types of therapeutic exercise

Therapeutic exercises aimed at achieving and maintaining physical fitness fall into the following major categories:

• Endurance training
• Resistance training
• Flexibility training

Patient education

Transcutaneous Electrical Nerve Stimulation

Transcutaneous electrical nerve stimulation (TENS) currently is one of the most commonly used forms of electroanalgesia. Hundreds of clinical reports exist concerning the use of TENS for various types of conditions, such as  (LBP), myofascial and arthritic pain, sympathetically mediated pain,  pain, visceral pain, and . Because many of these studies were uncontrolled, there has been ongoing debate about the degree to which TENS is more effective than placebo in reducing pain.^{[1, 2, 3, 4]}
The image below depicts a TENS unit.
TENS (Transcutaneous Electrical Nerve Stimulator). Image courtesy of Wikimedia Commons. The currently proposed mechanisms by which TENS produces neuromodulation include the following:

• Presynaptic inhibition in the dorsal horn of the spinal cord
• Endogenous pain control (via endorphins, enkephalins, and dynorphins)^[5]
• Direct inhibition of an abnormally excited nerve
• Restoration of afferent input

The results of laboratory studies suggest that electrical stimulation delivered by a TENS unit reduces pain through nociceptive inhibition at the presynaptic level in the dorsal horn, thus limiting its central transmission. The electrical stimuli on the skin preferentially activate low-threshold, myelinated nerve fibers. The afferent input from these fibers inhibits propagation of nociception carried in the small, unmyelinated C fibers by blocking transmission along these fibers to the target or T cells located in the substantia gelatinosa (laminae 2 and 3) of the dorsal horn.
Studies show marked increases in beta endorphin and met-enkephalin with low-frequency TENS, with demonstrated reversal of the antinociceptive effects by naloxone.^[6] These effects have been postulated to be mediated through micro-opioid receptors. Research indicates, however, that high-frequency TENS analgesia is not reversed by naloxone, implicating a naloxone-resistant, dynorphin-binding receptor. A sample of cerebral spinal fluid in those subjects demonstrated increased levels of dynorphin A.
The mechanism of the analgesia produced by TENS is explained by the gate-control theory proposed by Melzack and Wall in 1965.^[7] The gate usually is closed, inhibiting constant nociceptive transmission via C fibers from the periphery to the T cell. When painful peripheral stimulation occurs, however, the information carried by C fibers reaches the T cells and opens the gate, allowing pain transmission centrally to the thalamus and cortex, where it is interpreted as pain. The gate-control theory postulates a mechanism by which the gate is closed again, preventing further central transmission of the nociceptive information to the cortex. The proposed mechanism for closing the gate is inhibition of the C-fiber nociception by impulses in activated myelinated fibers.

Classification and Complications of Traumatic Brain Injury

Epidemiology

Traumatic brain injury (TBI), also known as acquired brain injury, head injury, or brain injury, causes substantial disability and mortality. It occurs when a sudden trauma damages the brain and disrupts normal brain function. TBI may have profound physical, psychological, cognitive, emotional, and social effects. The diagnosis of mild TBI appears to be vastly underdiagnosed in the setting of systemic trauma, even in trauma centers.^[1]
According to the Center for Disease Control and Prevention's National Center for Injury Prevention and Control, the following annual statistics apply in the United States^[2] :

• At least 1.4 million people sustain a TBI.
• Approximately 50,000 people die from a TBI.
• Approximately 475,000 TBIs occur among infants, children, and adolescents aged 0-14 years.
• About 80,000-90,000 people experience the onset of a long-term disability due to a TBI.

The following groups are at particular risk for TBI^[2] :

• Males are about twice as likely as females to sustain a TBI.
• Infants and children aged 0-4 and adolescents aged 15-19 years are the 2 age groups at highest risk for a TBI.
• Adults aged 75 years or older have the highest rates of TBI-related hospitalization and death.

A TBI is caused by an excessive force, blow, or penetrating injury to the head. The leading causes of TBI are as follows^[2] :

• Falls (28%)
• Motor vehicle crashes (20%)
• Being struck by or against objects (19%)
• Assaults (11%)

Mortality rates after brain injury are highest in people with a severe TBI. In the first year after a TBI, people who survive are more likely to die from seizures, septicemia, pneumonia, digestive conditions, and all external causes of injury than are other people of similar age, sex, and race.^[3] However, the mortality rate after severe TBI has decreased since the late 20th century.^[4]
In one study, researchers estimated that the economic burden of TBI in the United States was approximately $37.8 billion in 1985.^[5] This estimate included $4.5 billion in direct expenditures for hospital care, extended care, and other medical care and services; $20.6 billion in work-related losses and disability; and $12.7 billion in lost income from premature death.

Post Head Injury Autonomic Complications

Autonomic dysfunction syndrome (ADS) is reported in cases of brain injury (TBI), hydrocephalus,subarachnoid hemorrhage, and intracerebral hemorrhage. ADS is rarely reported without an identified cause. In ADS, altered autonomic activity results in  fever, tachycardia, tachypnea, pupillary dilation, and extensor posturing. In an effort to more precisely characterize this syndrome, a second term for it—paroxysmal autonomic instability with dystonia (PAID)—has come into use.
PAID occurs as a result of severe brain injury (Rancho level ≤ IV) from multiple causes, including traumatic brain injury (TBI), hydrocephalus, brain tumors, subarachnoid hemorrhage, and intracerebral hemorrhage. PAID is a syndrome attributed to altered autonomic activity. Clinical manifestations consist of a temperature of 38.5º C, hypertension, a pulse rate of at least 130 beats per minute, a respiratory rate of at least 140 breaths per minute, intermittent agitation, and diaphoresis; these are accompanied by dystonia (rigidity or decerebrate posturing for a duration of at least 1 cycle per d for at least 3 d).
Other issues that can occur because of autonomic dysregulation are electrocardiographic alterations, arrhythmias, increased intracranial pressure (ICP), hypohidrosis, subnormal temperature in flaccid limbs, and neurogenic lung disease. Usually episodic, PAID first appears in the intensive care setting but may persist into the rehabilitation phase for weeks to months after injury in individuals who remain in a low-response state.
See also the following related eMedicine topics:

Post Head Injury Endocrine Complications

The greatest challenge associated with endocrine complications in individuals with traumatic brain injury (TBI) is early recognition of these subtle problems. Endocrine complications can produce significant impact on the progress and outcome of TBI rehabilitation. Prompt diagnosis and treatment of endocrine complications following TBI facilitate the rehabilitation process of patients with TBI.^{[1, 2]}
The release of pituitary hormones, orchestrated by the neuropeptide signals from the hypothalamus, provides a tight control of hormone-regulated homeostasis. The pituitary gland is protected well within the sella turcica of the sphenoid bone; however, the pituitary stalk, connected to the anterior pituitary and hypothalamus, is vulnerable to the effects of TBI, especially in patients with associated facial fractures, cranial nerve injuries, and dysautonomia.

Posttraumatic Heterotopic Ossification

n 1918, Dejerine and Ceillier first described heterotopic ossification (HO) in paraplegic patients injured in World War I, referring to the process as paraosteoarthropathy. HO has been defined as the formation of mature lamellar bone in soft tissues. The process involves true osteoblastic activity and bone formation. HO has been reported in cases of brain injury, spinal cord injury, poliomyelitis, myelodysplasia, tabes dorsalis, carbon monoxide poisoning, spinal cord tumors, syringomyelia, tetanus, and  This condition also has been reported after burns and total hip replacement/joint .
Several terms have been used to describe the condition, including heterotopic ossification, ectopic ossification, and myositis ossificans. HO usually involves the large joints of the body (eg, hips, elbows, shoulders, knees). Excessive bone formation may result in significant disability by severely limiting the range of motion (ROM) of these joints (see image below).
This radiograph clearly demonstrates fairly extensive heterotopic ossification at the bilateral hip regions. The extensive bone formation shown here makes it easy for the viewer to understand why a patient with HO could present with complaints such as pain, swelling, palpable mass, and decreased range of motion. The following 3 categories of HO have been described:

• Myositis ossificans progressiva - This is a rare metabolic bone disease in children with progressive metamorphosis of skeletal muscle to bone; it is characterized by an autosomal dominant pattern of genetic transmission.
• Myositis ossificans circumscripta without  Also referred to as neurogenic HO, this is a localized soft-tissue ossification occurring after neurologic injury or burns.
• Traumatic myositis ossificans - This condition occurs from direct injury to the muscles. Fibrous, cartilaginous, and osseous tissues near bone are affected; the muscle may not be involved.

Related eMedicine topics:

Posttraumatic Hydrocephalus

Posttraumatic hydrocephalus (PTH) is a frequent and serious complication that follows a traumatic brain injury (TBI).^{[1, 2, 3]} Its incidence varies greatly from study to study, largely based on different criteria for its diagnosis. However, PTH could greatly impact morbidity following a TBI and could result in increased mortality if it is not recognized and treated.
PTH may result from 1 or a combination of pathophysiologic factors. It can be caused by the overproduction of cerebrospinal fluid (CSF), the blockage of normal CSF flow, or insufficient absorption that results in excessive accumulation of CSF around the brain. Ultimately, PTH is caused by an imbalance that occurs between CSF production and absorption.^[4]
PTH may present as normal pressure hydrocephalus (NPH) or as a syndrome of increased intracranial pressure.^[5] Because of differences in prognosis and treatment, PTH needs to be distinguished from cerebral atrophy (ie, hydrocephalus ex vacuo) and ventricular enlargement caused by a failure of brain development. If PTH goes unrecognized or untreated, increased morbidity or mortality following a TBI is more likely.^{[6, 7]}

Classification

Dandy and Blackfan introduced the classification of hydrocephalus as either noncommunicating or communicating.^[8] In noncommunicating hydrocephalus (also called obstructive hydrocephalus), CSF accumulates in the ventricles because of CSF flow blockage. As a result, the ventricles enlarge and the hemispheres expand. The following sites are prone to the obstruction of CSF flow^[9] :

• Foramen of Monro
• Third ventricle
• Aqueduct of Sylvius
• Fourth ventricle
• Foramen of Luschka
• Foramen of Magendie

Conversely, in communicating hydrocephalus (also referred to as nonobstructive hydrocephalus), full communication between the ventricles and the subarachnoid space exists. Impaired CSF absorption may cause communicating hydrocephalus. The apparent mechanism is partial occlusion of the arachnoid villi, perhaps by blood and inflammatory mediators. Severe skull fractures, hemorrhage, and meningitis may predispose patients to this variant of PTH.^[9] Portnoy proposed that PTH develops as a result of increased dural sinus pressure, causing decreased CSF outflow.^[10]
NPH, a form of communicating hydrocephalus, may result from subarachnoid hemorrhage caused by an aneurysm rupture or a TBI, encephalopathy, or . NPH often presents as the classic triad of a progressive gait disorder, impairment of mental function, and urinary incontinence.^[9] In NPH, ventricles enlarge despite normal or even slightly reduced intracranial pressure, and they continue to press against brain parenchyma.
See also the following related topic in Medscape:
Resource Center
See also the following related topics in eMedicine:

Adhesive Capsulitis in Physical Medicine and Rehabilitation

most commonly referred to as frozen shoulder (FS), is an idiopathic disease with 2 principal characteristics: pain and contracture.

Pain

Shoulder pain associated with FS is progressive and initially felt mostly at night or when the shoulder is moved close to the end of its range of motion (ROM). It can be caused by certain combined movements of the shoulder, such as abduction and external rotation (eg, grooming one's hair, reaching for a seatbelt overhead) or extension and internal rotation (eg, reaching for a back pocket or bra strap). The pain usually progresses to constant pain at rest that is aggravated by all movements of the shoulder and that may be worsened by repetitive movements of the involved upper extremity, psychological stress, exposure to cold or vibration, and changes in the weather. In approximately 90% of patients with FS, this pain usually lasts 1-2 years before subsiding.^[1]

Contracture

The second principal characteristic of FS is progressive loss of passive ROM (PROM) and active ROM (AROM) of the  in a capsular pattern. That is, the movements are usually restricted to a characteristic pattern, with proportionally greater passive loss of external rotation than of abduction and internal rotation.
In 1934, Codman stated, "This entity [FS] is difficult to define, difficult to treat, and difficult to explain from the point of view of pathology." Codman's statement continues to hold true today.
In 1992, the American Shoulder and Elbow Surgeons Society agreed on the following definition of FS by consensus: a condition of uncertain etiology that is characterized by clinically significant restriction of active and passive shoulder motion that occurs in the absence of a known intrinsic shoulder disorder

Biceps Rupture

Tendon ruptures of the biceps brachii, one of the dominant muscles of the arm, have been reported in the United States with increasing frequency. Ruptures of the proximal biceps tendon make up 90-97% of all biceps ruptures and almost exclusively involve the long head.

Anatomy

Because of its size and its orientation about the shoulder and elbow joints, the biceps muscle is involved in functional activities of the upper limb. At its proximal attachment, the biceps has 2 distinct tendinous insertions on the scapula from its long and short heads. The short head arises from the coracoid process with the coracobrachialis, while the long head originates from the supraglenoid tubercle and passes over the humeral head within the capsule of the glenohumeral joint (see image below).
Biceps muscle and tendons The biceps muscle then continues down the arm within the intertubercular groove, covered by a synovial outpouching of the joint capsule. The 2 muscle bellies unite near the midshaft of the humerus and attach distally on the radial tuberosity. The distal tendon blends with the bicipital aponeurosis, which affords protection to structures of the cubital fossa, allowing distribution of forces across the elbow to lessen the pull on the radial tuberosity.^{[1, 2]} The biceps receives innervation via the musculocutaneous nerve (C5, C6) from the lateral cord of the brachial plexus.

Carpal Tunnel Syndrome

Carpal tunnel syndrome (CTS) is a collection of characteristic symptoms and signs that occurs following entrapment of the median nerve within the carpal tunnel. Usual symptoms include numbness, paresthesias, and pain in the median nerve distribution. These symptoms may or may not be accompanied by objective changes in sensation and strength of median-innervated structures in the hand. See image below.
The hands of an 80-year-old woman with a several-year history of numbness and weakness are shown in this photo. Note severe thenar muscle (abductor pollicis brevis, opponens pollicis) wasting of the right hand, with preservation of hypothenar eminence

Heterotopic Ossification

The term heterotopic ossification (HO) describes bone formation at an abnormal anatomical site, usually in soft tissue. HO can be classified into the following 3 types:

• Myositis ossificans progressiva (fibrodysplasia ossificans progressiva) - This disorder is among the rarest genetic conditions, with an incidence of 1 case per 2 million persons. Transmission is autosomal dominant with variable expression. The condition is characterized by (a) recurrent, painful soft-tissue swelling that leads to HO and (b) congenital malformation of the great toe. There is no treatment for this form of HO. Limited benefits have been reported using corticosteroids and etidronate. Most patients die early from restricted lung disease and pneumonia; however some patients live productive lives.^[1]
• Traumatic myositis ossificans - In this condition, a painful area develops in muscle or soft tissue following a single blow to the area, a muscle tear, or repeated minor  The painful area gradually develops masses with a cartilaginous consistency; within 4-7 weeks, a solid mass of bone can be felt. Common sites include the pectoralis major, the biceps, and thigh muscles. A nontraumatic type of myositis ossificans also may exist.
• Neurogenic heterotopic ossification - This condition is the one that comes to mind when the generic phrase heterotopic ossification is used. This type of HO is the subject of this article. The various terms mentioned at the outset all refer to this type of HO.

In 1918, Dejerine and Ceilier first described HO in patients with spinal cord injury (SCI) from the First World War. Now HO is recognized as a fairly common sequela of SCI, especially [2

Olecranon Bursitis

Olecranon  a relatively common condition, is inflammation of the bursa overlying the olecranon process at the proximal aspect of the ulna (see the images below).^[1] The superficial location of the bursa, between the ulna and the skin at the posterior tip of the elbow, makes it susceptible to inflammation from acute or  Less commonly, inflammation results from infection (septic bursitis). (See Etiology, Workup, Treatment, and Medication.)^{[1, 2, 3, 4, 5]}
Olecranon bursitis, shown here with the elbow flexed. Image courtesy of UMDNJ-New Jersey Medical School, www.DoctorFoye.com, and www.TailboneDoctor.com. Olecranon bursitis seen with the elbow extended; the focal olecranon swelling is more visible than it is when the elbow is flexed. Image courtesy of UMDNJ-New Jersey Medical School, www.DoctorFoye.com, and www.TailboneDoctor.com. Olecranon bursitis seen with the elbow extended. Image courtesy of UMDNJ-New Jersey Medical School, www.DoctorFoye.com, and www.TailboneDoctor.com

Rotator Cuff Disease

In 1834, Smith wrote the first description of a rupture of the rotator cuff tendon. Since then, with the work of such authors as Duplay, Von Meyer, Codman, and Neer, degenerative changes to the rotator cuff have been better characterized; however, the exact mechanisms leading to the degeneration of the rotator cuff still are debated today.^{[1, 2, 3, 4, 5, 6, 7, 8]} Moreover, despite numerous trials, questions still exist about the efficacy of different therapeutic modalities for rotator cuff disease. With the help of better methodology for studies, more successful treatment of degenerative rotator cuff disease can be expected. See the images below.
Normal plain radiograph of the shoulder in internal, external, and neutral positions. This image depicts the channel between the articular capsule and the subacromial-subdeltoid bursa in a complete rotator cuff tear. Even if the channel cannot be always identified, the presence of contrast medium in the subdeltoid-subacromial bursa signs the presence of a complete rotator cuff tea

Shoulder Pain in Hemiplegia

Good shoulder function is a prerequisite for effective hand function, as well as for performing multiple tasks involving mobility, ambulation, and activities of daily living (ADL). A common sequela of stroke is hemiplegic shoulder pain that can hamper functional recovery and subsequently lead to disability. Poduri reports that hemiplegic shoulder pain can begin as early as 2 weeks poststroke but typically occurs within 2-3 months poststroke.^[1]
Most studies have speculated about the etiology of shoulder pain in hemiplegia but have failed to establish a cause-and-effect relationship. Some of the most frequently suspected factors contributing to shoulder pain include subluxation, contractures, complex regional pain syndrome (CRPS), rotator cuff injury, and spastic muscle imbalance of the glenohumeral joint.^[2]
However, identifying the exact mechanism(s) of shoulder pain can be inherently difficult, with many of the current treatment regimens varying according to assumptions made about its cause. Hanger and colleagues suggested it to be highly probable that the cause is multifactorial, with different factors contributing at different stages of recovery (ie, flaccidity contributing to subluxation and subsequent capsular stretch, abnormal tonal and synergy patterns contributing to rotator cuff or scapular instability).^[3] Because of the difficulty in treating shoulder pain once established, early initiation of treatment is valuable.
For individuals who have had strokes with resultant hemiplegia, motor and functional recovery are important steps in the treatment process. Chae and coauthors indicated that the amount of motor recovery is related to the degree of initial severity and the amount of time before voluntary movements are initiated.^{[4, 5]}
Numerous neurofacilitative treatments have been developed in hopes of improving the quality and decreasing the amount of time to recovery. Unfortunately, Chae et al found that the length of stay at most acute inpatient rehabilitation facilities is shortening; they also determined that the primary means of restoring maximal function involves the use of compensatory strategies, rather than the employment of motor control restoration.

Acute Compartment Syndrome

Acute compartment syndrome occurs when the tissue pressure within a closed muscle compartment exceeds the perfusion pressure and results in muscle and nerve ischemia. It typically occurs subsequent to a traumatic event, most commonly a fracture.
The cycle of events leading to acute compartment syndrome begins when the tissue pressure exceeds the venous pressure and impairs blood outflow. Lack of oxygenated blood and accumulation of waste products result in pain and decreased peripheral sensation secondary to nerve irritation.
Late manifestations of compartment syndrome include the absence of a distal pulse, hypoesthesia, and extremity paresis, because the cycle of elevating tissue pressure eventually compromises arterial blood flow. If left untreated or if inadequately treated, the muscles and nerve within the compartment undergo ischemic necrosis, and a limb contracture, called ults. Severe cases may lead to renal failure and death.
The literature is somewhat confusing because of the interchangeable use of the terms acute, subacute, chronic, and recurrent compartment syndrome; crush syndrome; and Volkmann ischemic contracture. Crush syndrome is distinct from compartment syndrome; it is defined as a severe systemic manifestation (eg, rhabdomyolysis) of trauma and ischemia involving soft tissues, principally skeletal muscle, as a result of prolonged severe crushing. Crush syndrome trauma or rhabdomyolysis may also lead to an acute compartment syndrome.
Chronic compartment syndrome (CCS) is a recurrent syndrome during exercise or work. CCS is characterized by pain and disability that subside when the precipitating activity is stopped but that return when the activity is resumed. Although CSS is more common in the anterior compartment of the lower leg, it has been described in the forearm of motocross racers and other athletes.^{[1, 2, 3]} For more information, see the Medscape Reference article
The incidence of compartment syndrome depends on the patient population studied and the etiology of the syndrome. In a study by Qvarfordt and colleagues, 14% of patients with leg pain were noted to have anterior compartment syndrome^[4] ; compartment syndrome was seen in 1-9% of leg fractures.
Compartment syndrome may affect any compartment, including the hand, forearm, upper arm,  buttock,^[5] and entire lower extremity. Almost any injury can cause this syndrome, including injury resulting from vigorous exercise. Clinicians need to maintain a high level of suspicion when dealing with complaints of extremity pain.^[6]
The definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release), with subsequent fracture reduction or stabilization and vascular repair, if needed. The goal of decompression is restoration of muscle perfusion within 6 hours. (See Treatment.)

Historical aspects

The original description of the consequences of unchecked rising intracompartmental pressures is widely attributed to Richard von Volkmann. His 1872 publication documented nerve injury and subsequent contracture from compartment syndrome following supracondylar fracture.^[7] That injury remains known as Volkmann contracture.
Although long bone fractures are a common cause of compartment syndrome, other injuries are also a common antecedent to compartment syndrome. Approximately 50 years after von Volkmann's seminal paper, Jepson described ischemic contractures in dog hind legs caused by limb hypertension after experimentally induced venous obstruction.^[8]
Wilson first described the initial case of exertional compartment syndrome in 1912. Mavor, in 1956, first reported a case of chronic compartment syndrome. Since then, various cases of compartment syndrome have been reported in the literature, and pathophysiology and treatment options have been discussed.
In 1941, Bywaters and Beall reported on the significance of crush injury while working with victims of the London Blitz. These pioneers revealed mechanisms and consequences of compartment syndrome. In the 1970s, the importance of measuring intracompartmental pressures became apparent.
Owen et al published a series of articles describing the use of the wick catheter for pressure measurement and then documented high compartmental pressures in various circumstances.^[9] Almost simultaneously, Matsen published his findings, which are the most commonly annotated group of articles in present literature.^[10]

Kugelberg Welander Spinal Muscular Atrophy

Spinal muscular atrophies (SMAs) represent a rare group of inherited disorders that cause progressive degeneration of the anterior horn cells of the spinal cord. The exact cause of the degeneration is unknown. Loss of these cells results in a progressive lower motor neuron disease that has no sensory involvement and that is manifested as hypotonia, weakness, and progressive paralysis. Kugelberg Welander spinal muscular atrophy (also known as Wohlfart-Kugelberg-Welander syndrome or mild SMA) is a milder form of SMA, with symptoms typically presenting after age 18 months.^{[1, 2, 3]}
SMAs were first described in the 1890s, by Guido Werdnig, a physician from the University of Vienna, in his lecture "On a Case of Muscular Dystrophy with Positive Spinal Cord Findings." Soon after, Professor Johann Hoffmann from Heidelberg University presented a paper describing a syndrome of progressive atrophy, weakness, and death during the early childhood period of siblings with genetically normal parents. Both physicians conducted autopsies on their patients and found severe atrophy of the ventral roots of the spinal cord. They also found histologic evidence of loss of motor neurons in the anterior horn cells of this region. Hoffmann called the syndrome spinale muskelatrophie (spinal muscular atrophy).
In the early 1960s, Byers and Banker classified SMA into categories based on the severity and age of onset of the symptoms, in an effort to predict prognosis. Their system, summarized below, became the basis for the most widely recognized system now used for the classification of SMA.

Hereditary Spastic Paraplegia

Hereditary spastic paraplegia (HSP) is not a single disease entity; it is a group of clinically and genetically diverse disorders that share a primary feature, which is the causation of progressive and generally severe lower extremity weakness and spasticity. (See Etiology, Presentation, and Workup.)
Strümpell first described hereditary forms of spastic paraplegia (see the image below) in 1883, with Lorrain later providing more extensive detail. HSP is also called familial spastic paraparesis and Strümpell-Lorrain syndrome. (See Presentation.)
Photograph of a 16-year-old girl with complicated hereditary spastic paraplegia. She has a spastic gait disturbance, mental retardation, and extrapyramidal symptoms. Note the dysmorphic features. Numerous clinical reports have documented that HSP syndromes are heterogeneous. Syndromes are classified as uncomplicated, or pure, when only spinal involvement occurs, and they are classified as complicated when they are associated with neurologic abnormalities, such as ataxia, mental retardation, dementia, extrapyramidal dysfunctions, visual or hearing dysfunctions,^[1] adrenal insufficiency, and ichthyosis. Clinical distinctions between pure and complicated forms of HSP have some utility. (See Prognosis, Presentation, Workup, Treatment, and Medication.)
The most useful classifications now are based on the mode of inheritance and genetic linkage. HSP may also be classified as autosomal dominant, autosomal recessive, or X-linked, and each type has several subtypes, which are based on the location of the gene. The mode of inheritance cannot be used to predict the severity of the disorder, however, because symptoms can vary greatly within each type. (See Etiology.)
In the past, HSP was also classified as type I or type II, based on the patient's age at the onset of symptoms and on the amount of spasticity versus weakness. Because both types can appear in the same family, this method of classification is no longer in general use. (The age of onset often has no clear relation to the HSP genotype.)^[2]
To date, the locations of several genes associated with HSP have been identified. Eighteen types of dominantly inherited pure or complicated HSP are known, along with 17 types of recessively inherited HSP and 3 types of X-linked HSP.^[3]

Complications

Patients with HSP may have several possible complications, including the following (see Prognosis):

• Gastrocnemius-soleus contracture
• Cold feet
• Fatigue
• Back and knee pain
• Stress and depression

Patient education

Amyotrophic Lateral Sclerosis (ALS) in Physical Medicine and Rehabilitation

s the most common type of adult-onset motor neuron disease. Adult-onset motor neuron diseases are a group of neurologic disorders that present in adult life and are characterized primarily by progressive degeneration and loss of motor neurons. ALS involves upper and lower motor neurons and presents as an idiopathic, progressive degeneration of anterior horn cells and their associated neurons, resulting in progressive muscle weakness, atrophy, and fasciculations.^{[1, 2]}
The disease was first described in 1869 and is commonly called Lou Gehrig disease, after the professional baseball player who died of ALS in 1941.
Other diseases classified as adult-onset motor neuron diseases have more restricted presentations and can evolve into idiopathic ALS if the patient is tracked for a long period. These diseases include the following:

• Progressive bulbar palsy - Pure bulbar involvement
• Progressive muscular atrophy - Pure lower motor neuron degeneration
• - Pure upper motor neuron degeneration
• Adult-onset spinal muscular atrophy - Includes a broad range of primary motor neuron diseases classified by pattern of inheritance, distribution of weakness, or age of onset

Respiratory complications

All deaths directly caused by ALS result from respiratory complications. This occurs primarily from the patient's inability to ventilate as respiratory muscle weakness progresses. In patients with bulbar weakness, aspiration of secretions or food may occur and precipitate pneumonia, resulting in further respiratory compromise; therefore, aggressive respiratory management is necessary in the comprehensive care of patients with ALS.
Routinely measure vital capacity in the sitting and recumbent positions. Most often, the recumbent measurement declines prior to the sitting measurement. Gravity assists in lowering the diaphragm as the patient's angle of inclination is increased. As respiratory weakness progresses, patients have increasing difficulty with diaphragmatic movement when supine because of the elimination of this effect from gravity. This results in alveolar hypoventilation and ultimate oxyhemoglobin desaturation.
Difficulty sleeping may be the first symptom of hypoventilation. Patients should be questioned routinely regarding sleep habits, and if a sleep disturbance develops, measure vital capacities sitting and supine. In addition, perform overnight oxygen saturation monitoring to assess for nocturnal hypoxemia and the need for nocturnal noninvasive intermittent positive pressure ventilation (IPPV).

Special concerns

An attorney should be consulted regarding a "living will" and power of attorney should be established prior to the terminal phase of this ultimately fatal disease.
Also see the following:

Acute Poliomyelitis

Acute poliomyelitis is a disease of the anterior horn motor neurons of the spinal cord and brain stem caused by poliovirus. Flaccid asymmetric weakness and muscle atrophy are the hallmarks of its clinical manifestations, due to loss of motor neurons and denervation of their associated skeletal muscles. Because of the success of poliovirus vaccine, poliomyelitis, once one of the most feared human infectious diseases, is now almost entirely preventable by proper immunization (see image below).
The typical contractures of postpolio residual paralysis. In 1988, the World Health Organization initiated the Global Polio Eradication Initiative to eradicate poliomyelitis; at the time, it was endemic in 125 countries. As of 2006, only 6 countries were endemic for polio; however, the worldwide campaign to eradicate polio continues today, as do efforts to prevent transmission of the disease into polio-free areas.

Cervical Sprain and Strain

Cervical strain is one of the most common musculoskeletal problems encountered by generalists and neuromusculoskeletal specialists in the clinic.
A normal and straightened lordatic curve are shown below.
Radiograph of the cervical spine shows a normal lordotic curve. Radiograph of the cervical spine shows straightening of the lordotic curve. One cause of cervical strain is termed cervical acceleration-deceleration injury; this is frequently called whiplash injury.
Whiplash, one of the most common sequela of nonfatal car injuries, is one of the most poorly understood disorders of the spine, and the severity of the  is often not correlated with the seriousness of the clinical problems.^[1] A history of neck injury is a significant risk factor for chronic neck pain.^[2] Pretorque of the head and neck increases facet capsular strains, supporting its role in the whiplash mechanism.^[3]
The Quebec Taskforce on Whiplash-Associated Disorders has suggested the following system for classifying the severity of cervical sprains^[4] :

• 0 - No neck pain complaints, no physical signs
• 1 - Neck pain complaints, only stiffness or tenderness, no other physical signs
• 2 - Neck complaints and musculoskeletal signs (decreased range of motion [ROM] and point tenderness)
• 3 - Neck complaints and neurologic signs (weakness, sensory and reflex changes)
• 4 - Neck complaints with and/or dislocation

Cervical Myofascial Pain

Pain attributed to muscle and its surrounding fascia is termed myofascial pain, with cervical myofascial pain thought to occur following either overuse or trauma to the muscles that support the shoulders and neck. In the cervical spine, the muscles most often implicated in myofascial pain are the trapezius, levator scapulae, rhomboids, supraspinatus, and infraspinatus. (See Etiology.)^[1]
Myofascial pain in any location is characterized on examination by the presence of trigger points located in skeletal muscle. A trigger point is defined as a hyperirritable area located in a palpable, taut band of muscle fibers (see the image below). (See Etiology, Presentation, and Treatment.)
Schematic of a trigger point complex of a muscle in longitudinal section. A: The central trigger point (CTrP) in the endplate zone contains numerous electrically active loci and numerous contraction knots. A taut band of muscle fibers extends from the trigger point to the attachment at each end of the involved fibers. The sustained tension that the taut band exerts on the attachment tissues can induce a localized enthesopathy that is identified as an attachment trigger point (ATrP). B: Enlarged view of part of the CTrP shows the distribution of 5 contraction knots. The vertical lines in each muscle fiber identify the relative spacing of its striations. The space between 2 striations corresponds to the length of 1 sarcomere. The sarcomeres within one of these enlarged segments (ie, contraction knot) of a muscle fiber are markedly shorter and wider than the sarcomeres in the neighboring normal muscle fibers, which are free of contraction knots. Descriptions of myofascial pain date back to the mid-19th century, when Froriep described muskelschwiele, or muscle calluses. He characterized these calluses as tender areas in muscle that felt like a cord or band associated with rheumatic complaints. In the early 1900s, Gowers first used the term fibrositis to describe muscular rheumatism associated with local tenderness and regions of palpable hardness.
In 1938, Kellgren described areas of referred pain associated with tender points in muscle. In the 1940s, Janet Travell, MD, began writing about myofascial trigger points. Her text, written in conjunction with David Simons, MD, continues to be viewed as the foundational literature on the subject of myofascial pain.^[2]
The primary concern for patients with cervical myofascial pain is chronicity. Recurrence of myofascial pain is a common scenario. Prompt treatment prevents other muscles in the functional unit from compensating and, consequently, producing a more widespread and chronic problem. Migraine headaches and muscle contraction headaches are known to occur frequently in the patient with myofascial pain.^[3] Temporomandibular joint (TMJ) syndrome also may be myofascial in origin. (See Prognosis, Presentation, Treatment, and Medication.)

Overview of Osteoarthritis Rehabilitation

Osteoarthritis (OA) is a chronic disease process affecting synovial joints, particularly large weight-bearing joints. OA is particularly common in older patients but can occur in younger patients either through a genetic mechanism or, more commonly, because of previous joint trauma.
Rehabilitation for patients with OA can be provided in various forms, including the following:

• Physical therapy
• Occupational therapy
• Medication
• Intra-articular injections
• Surgery

Cervical Disc Disease

Cervical disc disorders encountered in physiatric practice include   (HNP),  (DDD), and internal disc disruption (IDD). HNP (seen in the image below) is defined as localized displacement of nucleus, cartilage, fragmented apophyseal bone, or fragmented anular tissue beyond the intervertebral disc space.^[1] Most of the herniation is made up of the annulus fibrosus. DDD involves degenerative annular tears, loss of disc height, and nuclear degradation. IDD describes annular fissuring of the disc without external disc deformation. can result from nerve root injury in the presence of disc herniation or stenosis, most commonly foraminal , leading to sensory, motor, or reflex abnormalities in the affected nerve root distribution.^{[2, 3]}
Sagittal magnetic resonance imaging (MRI) scan demonstrating cervical intervertebral disc protrusions at C3-C4 and C7-T1. Understanding  requires basic knowledge of anatomy and biomechanics. The intervertebral disc is a functional unit connecting 2 vertebral bodies of the spine. The disc absorbs shock, accommodates movement, provides support, and separates vertebral bodies to lend height to intervertebral foramina. The disc consists of 3 structural components; an eccentrically located nucleus pulposus, a surrounding lamellar annulus fibrosus, and 2 cartilaginous endplates, separating each segmental level between the C2-T1 vertebrae. No disc exists between C1 and C2, and only ligaments and joint capsules resist excessive motion. Disc degeneration and/or herniation can injure the spinal cord or nerve roots and result in 

Physical Medicine and Rehabilitation for Systemic Lupus Erythematosus

SLE) is an inflammatory connective tissue disease with variable manifestations (eg, rash; see the images below).^{[1, 2, 3]} SLE may affect many organ systems with immune complexes and a large array of autoantibodies, particularly antinuclear antibodies (ANAs).The classic malar rash, also known as a butterfly rash, of systemic lupus erythematosus, with distribution over the cheeks and nasal bridge. Note that the fixed erythema, sometimes with mild induration as seen here, characteristically spares the nasolabial folds. Photosensitive systemic lupus erythematosus rashes typically occur on the face or extremities, which are sun-exposed regions. Photo courtesy of Dr. Erik Stratman, Marshfield Clinic.
Physical medicine and rehabilitation for SLE may involve physical therapy, occupational therapy, speech therapy, recreational therapy, or combinations thereof. Follow-up medical care of patients with SLE must be ongoing. One physician should coordinate the patient’s care. The physician and the patient must be alert to subtle changes in symptoms that may indicate a flare-up in the disease process.

Physical Medicine and Rehabilitation for Iliotibial Band Syndrome

Iliotibial band syndrome (ITBS) is the result of inflammation and irritation of the distal portion of the iliotibial tendon as it rubs against the lateral femoral condyle, or less commonly, the greater tuberosity. This  occurs with repetitive flexion and extension of the knee. Inflammation and irritation of the iliotibial band (ITB) also may occur because of a lack of flexibility of the ITB, which can result in an increase in tension on the ITB during the stance phase of running. See the image below.
In this 27-year-old female marathon runner with anterolateral pain superior to the joint line, a coronal fast spin-echo T2-weighted magnetic resonance imaging scan with fat suppression demonstrates edema between the iliotibial band and the lateral femoral condyle (arrow). The edema's location is consistent with a clinical diagnosis of iliotibial band syndrome. Other causes or factors that are believed to predispose an athlete to ITBS include excessive internal tibial rotation, genu varum, and increased pronation of the foot.